国际眼科纵览
國際眼科縱覽
국제안과종람
OREIGN MEDICAL SCIENCES
2012年
2期
116-121
,共6页
青光眼滤过手术%瘢痕化%转化生长因子-β
青光眼濾過手術%瘢痕化%轉化生長因子-β
청광안려과수술%반흔화%전화생장인자-β
glaucoma filtration surgery%scarring%transforming growth factor-beta
青光眼滤过术后滤过泡瘢痕化是手术失败的最主要原因.转化生长因子-β( TGF-β)能诱导人Tenon囊成纤维细胞表型转化,进一步迁移、增殖,合成细胞外基质,与滤过泡瘢痕化有重要关系.近年来在细胞因子及基因水平抗纤维化方面的研究取得一定进展,通过TGF-β抗体(如重组抗人TGF-β2单克隆抗体、CAT-152)、TGF-β抑制剂(如Decorin、糜酶抑制剂、SB-431542等)以及基因水平(如TGF-β的反义寡核苷酸等)来抑制TGF-β信号通路(如ALK5/Smad2/Smad3通路、MAPK通路、Rho-ROCK通路、PI3 K-AKT通路等)的重要靶点或蛋白表达,从而达到调控滤过泡瘢痕形成的作用.但目前很多药物的应用均缺乏临床试验支持,同时也缺少不同药物比较的研究.探索TGF-β细胞信号转导不同通路之间的关系,并寻找调控滤过道瘢痕化的最佳靶点是今后的研究方向.
青光眼濾過術後濾過泡瘢痕化是手術失敗的最主要原因.轉化生長因子-β( TGF-β)能誘導人Tenon囊成纖維細胞錶型轉化,進一步遷移、增殖,閤成細胞外基質,與濾過泡瘢痕化有重要關繫.近年來在細胞因子及基因水平抗纖維化方麵的研究取得一定進展,通過TGF-β抗體(如重組抗人TGF-β2單剋隆抗體、CAT-152)、TGF-β抑製劑(如Decorin、糜酶抑製劑、SB-431542等)以及基因水平(如TGF-β的反義寡覈苷痠等)來抑製TGF-β信號通路(如ALK5/Smad2/Smad3通路、MAPK通路、Rho-ROCK通路、PI3 K-AKT通路等)的重要靶點或蛋白錶達,從而達到調控濾過泡瘢痕形成的作用.但目前很多藥物的應用均缺乏臨床試驗支持,同時也缺少不同藥物比較的研究.探索TGF-β細胞信號轉導不同通路之間的關繫,併尋找調控濾過道瘢痕化的最佳靶點是今後的研究方嚮.
청광안려과술후려과포반흔화시수술실패적최주요원인.전화생장인자-β( TGF-β)능유도인Tenon낭성섬유세포표형전화,진일보천이、증식,합성세포외기질,여려과포반흔화유중요관계.근년래재세포인자급기인수평항섬유화방면적연구취득일정진전,통과TGF-β항체(여중조항인TGF-β2단극륭항체、CAT-152)、TGF-β억제제(여Decorin、미매억제제、SB-431542등)이급기인수평(여TGF-β적반의과핵감산등)래억제TGF-β신호통로(여ALK5/Smad2/Smad3통로、MAPK통로、Rho-ROCK통로、PI3 K-AKT통로등)적중요파점혹단백표체,종이체도조공려과포반흔형성적작용.단목전흔다약물적응용균결핍림상시험지지,동시야결소불동약물비교적연구.탐색TGF-β세포신호전도불동통로지간적관계,병심조조공려과도반흔화적최가파점시금후적연구방향.
Bleb scarring is the main cause of glaucoma filtration surgery failure. Transforming growth factor-beta (TGF-β) can induce the phenotypic modulation of human Tenon's capsule fibroblasts,then cause further migration,proliferation of the cells,synthesis of extracellular matrix,and eventually lead to the scarring of the bleb.There had been a lot of researchs at cytokine and gene level in antifibrotic area in recent years,which include TGF-β antibodies (such as anti-TGF-β2 antibody,CAT-152),TGF-β inhibitors (such as decorin,chymase inhibitor,SB-431542,etc.) and genetic level reagents (such as TGF-β antisense oligonucleotides,etc.) to inhibit the important target and protein expression in TGF-β signaling pathways (such as ALK5/Smad2/Smad3,MAPK,Rho-ROCK,PI3K-AKT signaling pathways,etc.),so as to achieve the role of reducing bleb scarring.But most of these drugs were lack of clinical trials support and of comparative studies among different drugs.Therefore,in-depth studies are still needed to explore the relationship among TGF-β cell signaling pathways,and find the best target for the regulation of bleb scarring.